Lourdes Siqueiros‐Márquez

Universidad Nacional Autónoma de México

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Carmen Clapp

Universidad Nacional Autónoma de México

Gonzálo Martínez de la Escalera

Universidad Nacional Autónoma de México

Cecilia Montáñez

Instituto Politécnico Nacional

Elva Adán‐Castro

Universidad Nacional Autónoma de México

Gabriela Ramírez‐Hernández

Harvard University

ÁR

Álvaro Rendón

Inserm

José‐Alain Sahel

Inserm

Francisco Freinet Núñez

Universidad Nacional Autónoma de México

Jakob Triebel

Nuremberg Hospital

Thomas Bertsch

Nuremberg Hospital

Cooperative Institutions

Universidad Nacional Autónoma de México

Centre National de la Recherche Scientifique

Inserm

Institut de la Vision

Autonomous University of Queretaro

Sorbonne Université

Instituto Mexicano de Oftalmología IAP

Université Paris Cité

Instituto Politécnico Nacional

Center for Research and Advanced Studies of the National Polytechnic Institute

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Role of Dexamethasone preventing Müller glial cells swelling

Investigative Ophthalmology & Visual Science (2016)

Lourdes Siqueiros‐Márquez Hugo Charles‐Messance Rodrigo Bolaños Cecilia Montáñez José‐Alain Sahel

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Vasoinhibin is Generated by the Renin-Angiotensin System

bioRxiv (Cold Spring Harbor Laboratory) (2024)

Francisco Freinet Núñez Lourdes Siqueiros‐Márquez Elva Adán‐Castro Magdalena Zamora Juan Pablo Robles

ABSTRACT Vasoinhibin is a fragment of the hormone prolactin (PRL) that inhibits angiogenesis, vasopermeability, and vasodilation. Cathepsin D (CTSD) cleaves the N-teminal of PRL to generate vasoinhibin in the retina of neonate mice as revealed by the CTSD inhibitor, pepstatin A (PA). However, PA also inhibits renin. Because renin is expressed in the retina and the renin-angiotensin system (RAS) gives rise to peptides with positive and negative effects on blood vessel growth and function, we investigated whether renin cleaves PRL to vasoinhibin in the newborn mouse retina and in the circulation. Newborn mouse retinal extracts from wild-type and CTSD-null newborn mice cleaved PRL to a 14 kDa vasoinhibin and such cleavage was prevented by heat-inactivation, PA, and the selective renin inhibitor VTP-27999 suggesting the contribution of renin. In agreement, recombinant renin cleaved different species PRLs to the expected 14 kDa vasoinhibin, a mass consistent with a consensus renin cleavage site located at Leu124-Leu125 in rat and mouse PRLs and at Leu126-Leu127 in human, bovine, and ovine PRLs. Dehydration and rehydration (D/R) in rats increased the levels of renin and PRL in plasma. Further increase in PRL circulating levels by the dopamine D2 receptor blocker, sulpiride, enabled detection of 14 kDa vasoinhibin in D/R rats. Moreover, the incubation of PRL with plasma from D/R rats generated a 14 kDa vasoinhibin that was prevented by VTP-27999. These findings add renin to the list of PRL-cleaving proteases and introduce vasoinhibin as a RAS-mediated mechanism for regulating blood vessel growth and function.

10.1101/2024.12.04.626908

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Prolactin improves retinal function in streptozotocin-induced diabetes

Investigative Ophthalmology & Visual Science (2020)

Lourdes Siqueiros‐Márquez Elva Hortencia Adan Castro Francisco Freinet Núñez Gabriela Ramírez‐Hernández Daniela Granados-Carrasco

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Embryonic neural stem/progenitor cells as model to characterize dystrophin and dystrophin-associated proteins expression during neuronal or astrocytic differentiation

MethodsX (2021)

José Romo‐Yáñez Griselda Rodríguez‐Martínez Jorge Aragón Lourdes Siqueiros‐Márquez Alma Herrera‐Salazar

Neural stem/progenitor cells (NSPC) are multipotent cells that renew themselves and could differentiate into neurons and macro glia (astrocytes and oligodendrocytes) of the nervous system during embryonic development. Duchenne muscular dystrophy is a severe type of muscular dystrophy caused by mutations in the dmd gene, and one-third of patients cursed with neuro-cognitive impairments. In this data article, we take advantage of the differentiation capacity of NSPC as a model to increase our knowledge in the neuronal and/or astrocytic differentiation and to evaluate the expression of dystrophins and dystrophin-associated proteins. We showed the characterization of undifferentiated and neuron and/or astrocyte differentiated NSPC. In addition, we evaluated the expression and subcellular localization of dystrophins and β-dystroglycan in undifferentiated NSPC and differentiated to neurons and astrocytes.•Primary culture of NSPC was characterized by the expression of multipotent markers nestin and Sox2.•Neuronal or astrocytic differentiation of NSPC was performed by basic fibroblast growth factor (FGF2) withdrawal, histamine or ciliary neurotrophic factor (CNTF) treatment, and expression of βIII-tubulin or glial fibrillary acidic protein (GFAP) as differentiation markers for neurons or astrocytes was evaluated.•This study will contribute to the understanding of dystrophins and dystrophin-associated proteins expression and function during neuronal or astrocytic differentiation of NSPC

Ciliary neurotrophic factor

Neuroepithelial cell

10.1016/j.mex.2021.101325

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Sulpiride‐induced hyperprolactinaemia increases retinal vasoinhibin and protects against diabetic retinopathy in rats

Journal of Neuroendocrinology (2022)

Elva Adán‐Castro Lourdes Siqueiros‐Márquez Gabriela Ramírez‐Hernández Nundehui Díaz‐Lezama Xarubet Ruíz‐Herrera

Excessive vasopermeability and angiogenesis compromise vision in diabetic macular oedema (DME) and diabetic retinopathy (DR). Vasoinhibin is a fragment of the hormone prolactin (PRL) that inhibits diabetes-induced retinal hypervasopermeability and ischaemia-induced retinal angiogenesis in rodents. Hyperprolactinaemia generated by the dopamine D2 receptor antagonist, levosulpiride, is associated with higher levels of vasoinhibin in the vitreous of patients with DR, implying a beneficial outcome due to vasoinhibin-mediated inhibition of retinal vascular alterations. Here, we tested whether hyperprolactinaemia induced by racemic sulpiride increases intraocular vasoinhibin levels and inhibits retinal hypervasopermeability in diabetic rats. Diabetes was generated with streptozotocin and, 4 weeks later, rats were treated for 2 weeks with sulpiride or osmotic minipumps delivering PRL. ELISA, Western blot, and Evans blue assay were used to evaluate serum PRL, retinal vasoinhibin, and retinal vasopermeability, respectively. Hyperprolactinaemia in response to sulpiride or exogenous PRL was associated with increased levels of vasoinhibin in the retina and reduced retinal hypervasopermeability. Furthermore, sulpiride decreased retinal haemorrhages in response to the intravitreal administration of vascular endothelial growth factor (VEGF). Neither sulpiride nor exogenous PRL modified blood glucose levels or bodyweight. We conclude that sulpiride-induced hyperprolactinaemia inhibits the diabetes- and VEGF-mediated increase in retinal vasopermeability by promoting the intraocular conversion of endogenous PRL to vasoinhibin. These findings support the therapeutic potential of sulpiride and its levorotatory enantiomer, levosulpiride, against DME and DR.

Sulpiride

Hyperprolactinaemia

10.1111/jne.13091

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Citations (9)

Immunolocalization of Gap Junction Protein Connexin 43 (GJA1) in retina and Glial Müller Cells in WT and Dp-71 null mice

Investigative Ophthalmology & Visual Science (2016)

Rodrigo Bolaños Lourdes Siqueiros‐Márquez Yonathan Garfias Cecilia Montáñez José‐Alain Sahel

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The dystrophin isoform Dp71eΔ71 is involved in neurite outgrowth and neuronal differentiation of PC12 cells

Journal of Proteomics (2018)

César García-Cruz Candelaria Merino‐Jiménez Vı́ctor Ceja Jorge Aragón Lourdes Siqueiros‐Márquez

Neurite

10.1016/j.jprot.2018.03.027

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Citations (9)

Protection of Glial Müller Cells by Dexamethasone in a Mouse Model of Surgically Induced Blood-Retinal Barrier Breakdown.

HAL (Le Centre pour la Communication Scientifique Directe) (2017)

Lourdes Siqueiros‐Márquez Romain Bénard Ophélie Vacca Hugo Charles‐Messance Rodrigo Bolaños-Jiménez

Breakdown of the inner blood-retinal barrier (iBRB) occurs in many retinal disorders and may cause retinal edema often responsible for vision loss. Dexamethasone is used in clinical practice to restore iBRB. The aim of this study was to characterize the impact of a surgically induced iBRB breakdown on retinal homeostatic changes due to dystrophin Dp71, aquaporin-4 (AQP4), and Kir4.1 alterations in Müller glial cells (MGC) in a mouse model. The protective effect of dexamethasone was assessed in this model. Moreover, retinal explants were used to control MGC exposure to a hypoosmotic solution containing barium.Partial lens surgery was performed in C57BL6/J mice. Dystrophin Dp71, AQP4, and Kir4.1 expression was analyzed by quantitative RT-PCR, Western blot, and immunohistochemistry. Twenty-four hours after surgery, mice received a single intravitreal injection of dexamethasone or of vehicle.After partial lens surgery, iBRB permeability increased while Dp71 and AQP4 were downregulated and Kir4.1 was delocalized. These effects were partially prevented by dexamethasone injection. In the retinal explant model, MGC were swollen and Dp71, AQP4, and Kir4.1 were downregulated after exposure to a hypoosmotic solution containing barium, but not in the presence of dexamethasone. Heat shock factor protein 1 (HSF1) was overexpressed in dexamethasone-treated retinas.Partial lens surgery induces iBRB breakdown and molecular changes in MGC, including a downregulation of Dp71 and AQP4 and the delocalization of Kir4.1. Dexamethasone seems to protect retina from these molecular changes by upregulating HSF1.

10.1167/iovs.16-20617

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Citations (8)

Prolactin stimulates the vascularisation of the retina in newborn mice under hyperoxia conditions

Journal of Neuroendocrinology (2020)

Miguel Vázquez‐Membrillo Lourdes Siqueiros‐Márquez Francisco Freinet Núñez Nundehui Díaz‐Lezama Elva Adán‐Castro

The hormone prolactin (PRL) is emerging as an important regulator of ocular blood vessels. PRL is pro-angiogenic and acquires anti-angiogenic properties after undergoing proteolytic cleavage to the PRL fragment, vasoinhibin. The vascularisation of the rodent retina develops after birth when it rapidly expands until completion at the end of the first postnatal week. Exposure of newborn mice to high oxygen levels lowers the rate of blood vessel growth. In the present study, we investigated whether PRL treatment modifies the vascularisation of the retina in newborn mice exposed to high oxygen or to normoxia and whether the retinal conversion of PRL to vasoinhibin may be altered in the neonate. Newborn mice and their nursing mothers were subjected to 75% oxygen or to normoxia from postnatal day (P) 6 to P8 (group 1) or from P2 to P5 (group 2). PRL (2 µg g

Hyperoxia

10.1111/jne.12858

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Citations (7)

Altered astrocyte morphology and vascular development in dystrophin‐Dp71‐null mice

Glia (2015)

Audrey Giocanti-Aurégan Ophélie Vacca Romain Bénard Sijia Cao Lourdes Siqueiros‐Márquez

Understanding retinal vascular development is crucial because many retinal vascular diseases such as diabetic retinopathy (in adults) or retinopathy of prematurity (in children) are among the leading causes of blindness. Given the localization of the protein Dp71 around the retinal vessels in adult mice and its role in maintaining retinal homeostasis, the aim of this study was to determine if Dp71 was involved in astrocyte and vascular development regulation. An experimental study in mouse retinas was conducted. Using a dual immunolabeling with antibodies to Dp71 and anti-GFAP for astrocytes on retinal sections and isolated astrocytes, it was found that Dp71 was expressed in wild-type (WT) mouse astrocytes from early developmental stages to adult stage. In Dp71-null mice, a reduction in GFAP-immunopositive astrocytes was observed as early as postnatal day 6 (P6) compared with WT mice. Using real-time PCR, it was showed that Dp71 mRNA was stable between P1 and P6, in parallel with post-natal vascular development. Regarding morphology in Dp71-null and WT mice, a significant decrease in overall astrocyte process number in Dp71-null retinas at P6 to adult age was found. Using fluorescence-conjugated isolectin Griffonia simplicifolia on whole mount retinas, subsequent delay of developing vascular network at the same age in Dp71-null mice was found. An evidence that the Dystrophin Dp71, a membrane-associated cytoskeletal protein and one of the smaller Duchenne muscular dystrophy gene products, regulates astrocyte morphology and density and is associated with subsequent normal blood vessel development was provided.

Muller glia

10.1002/glia.22956

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Citations (24)